Botulism 

Updated: Feb 15, 2019
Author: Kirk M Chan-Tack, MD; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD 

Overview

Practice Essentials

Botulism is an acute neurologic disorder that causes potentially life-threatening neuroparalysis due to a neurotoxin produced by Clostridium botulinum. The 3 main clinical presentations of botulism are as follows:

  • Infant botulism

  • Foodborne botulism

  • Wound botulism

Signs and symptoms

More than 90% of patients with botulism have 3-5 of the following signs or symptoms:

  • Nausea

  • Vomiting

  • Dysphagia

  • Diplopia

  • Dilated/fixed pupils

  • Extremely dry mouth unrelieved by drinking fluids

Generally, botulism progresses as follows:

  • Preceding or following the onset of paralysis are nonspecific findings such as nausea, vomiting, abdominal pain, malaise, dizziness, dry mouth, dry throat, and, occasionally, sore throat

  • Cranial nerve paralysis manifests as blurred vision, diplopia, ptosis, extraocular muscle weakness or paresis, fixed/dilated pupils, dysarthria, dysphagia, and/or suppressed gag reflex

  • Additional neurologic manifestations include symmetrical descending paralysis or weakness of motor and autonomic nerves

  • Respiratory muscle weakness may be subtle or progressive, advancing rapidly to respiratory failure

The autonomic nervous system is also involved in botulism, with manifestations that include the following:

  • Paralytic ileus advancing to severe constipation

  • Gastric dilatation

  • Bladder distention advancing to urinary retention

  • Orthostatic hypotension

  • Reduced salivation

  • Reduced lacrimation

Other neurologic findings include the following:

  • Changes in deep tendon reflexes, which may be either intact or diminished

  • Incoordination due to muscle weakness

  • Absence of pathologic reflexes and normal findings on sensory and gait examinations

  • Normal results on mental status examination

See Clinical Presentation for more detail.

Diagnosis

A mouse neutralization bioassay confirms botulism by isolating the botulinum toxin. Toxin may be identified in the following:

  • Serum

  • Stool

  • Vomitus

  • Gastric aspirate

  • Suspected foods

C botulinum may be grown on selective media from samples of stool or foods. Note that the specimens for toxin analysis should be refrigerated, but culture samples of C botulinum should not be refrigerated. Wound cultures that grow C botulinum suggest the presence of wound botulism.

Electromyography

Characteristic electromyographic findings in patients with botulism include the following:

  • Brief, low-voltage compound motor-units

  • Small M-wave amplitudes

  • Overly abundant action potentials

An incremental increase in M-wave amplitude with rapid repetitive nerve stimulation may help to localize the disorder to the neuromuscular junction.

See Workup for more detail.

Management

Rigorous and supportive care, including use of the following, is essential in patients with botulism:

  • Meticulous airway management - Of paramount importance, since respiratory failure is the most important threat to survival in patients with botulism

  • Cathartics and enemas - Administered to patients with bowel sounds to remove unabsorbed botulinum toxin from the intestine

  • Stress ulcer prophylaxis - A standard component of intensive care management

  • Nasogastric suction and intravenous hyperalimentation - Helpful if an ileus is present; if no ileus is present, tube feeding can be used for nutritional supplementation

  • Foley catheter - Often used to treat bladder incontinence; the catheter must be monitored conscientiously and changed regularly

  • Antibiotic therapy - Useful in wound botulism, but has no role in foodborne botulism

Magnesium salts, citrate, and sulfate should not be administered, because magnesium can potentiate the toxin-induced neuromuscular blockade.

Wound botulism requires the following:

  • Incision and thorough debridement of the infected wound

  • Antitoxin therapy

  • High-dose intravenous penicillin therapy

Prevention of nosocomial infections

Measures to reduce the risk of nosocomial infections include the following:

  • Close observation for hospital-acquired infections - Especially pneumonia (particularly aspiration pneumonia); precaution against aspiration is also necessary

  • Close observation for urinary tract infection

  • Meticulous skin care - To prevent decubital ulcers and skin breakdown

Careful attention to peripheral and central intravenous catheters with regular site rotation to reduce the risks of thrombophlebitis, cellulitis, and line infections should be part of the patient’s supportive care.

See Treatment and Medication for more detail.

Background

Botulism is an acute neurologic disorder that causes potentially life-threatening neuroparalysis due to a neurotoxin produced by Clostridium botulinum. The toxin binds irreversibly to the presynaptic membranes of peripheral neuromuscular and autonomic nerve junctions. Toxin binding blocks acetylcholine release, resulting in weakness, flaccid paralysis, and, often, respiratory arrest. Cure occurs following sprouting of new nerve terminals.

The 3 main clinical presentations of botulism include infant botulism (IB), foodborne botulism (FBB), and wound botulism (WB). Additionally, because of the potency of the toxin, the possibility of botulism as a bioterrorism agent or biological weapon is a great concern.[1] For more information, see CBRNE – Botulism.

Infant botulism is caused by ingested C botulinum spores that germinate in the intestine and produce toxin. These spores typically come from bee honey or the environment. Most infants fully recover with supportive treatment; the attributed infant mortality rate is less than 1%. Improperly canned or home-prepared foods are common sources of the toxin that can result in foodborne botulism. Wound botulism results from contamination of a wound with toxin-producing C botulinum. Foodborne botulism and wound botulism occur predominantly in adults and are the focus of this article.

C botulinum is an anaerobic gram-positive rod that survives in soil and marine sediment by forming spores. Under anaerobic conditions that permit germination, it synthesizes and releases a potent exotoxin. Microbiologically, the organism stains gram-positive in cultures less than 18 hours old. The organism may stain gram-negative after 18 hours of incubation, potentially complicating attempts at diagnosis. On a molecular weight basis, botulinum toxins are the most potent toxins known.

Eight antigenically distinct C botulinum toxins are known, including A, B, C (alpha), C (beta), D, E, F, and G. Each strain of C botulinum can produce only a single toxin type. Types A, B, E, and, rarely, F cause human disease. Toxins A and B are the most potent, and the consumption of small amounts of food contaminated with these types has resulted in full-blown disease. During the last 20 years, toxin A has been the most common cause of foodborne outbreaks; toxins B and E follow in frequency. In 15% of C botulinum infection outbreaks, the toxin type is not determined. Toxins C and D cause disease in various animals. Type G toxin has been associated with sudden death but not with neuroparalytic illness. It was isolated from autopsy material from 5 patients in Switzerland in 1977.

Pathophysiology

The mechanism of action involves toxin-mediated blockade of neuromuscular transmission in cholinergic nerve fibers. This is accomplished by either inhibiting acetylcholine release at the presynaptic clefts of the myoneural junctions or by binding acetylcholine itself. Toxins are absorbed from the stomach and small intestine, where they are not denatured by digestive enzymes. Subsequently, they are hematogenously disseminated and block neuromuscular transmission in cholinergic nerve fibers. The nervous, gastrointestinal, endocrine, and metabolic systems are predominantly affected.

Because the motor end plate responds to acetylcholine, botulinum toxin ingestion results in hypotonia that manifests as descending symmetric flaccid paralysis and is usually associated with gastrointestinal symptoms of nausea, vomiting, and diarrhea. Cranial nerves are affected early in the disease course. Later complications include paralytic ileus, severe constipation, and urinary retention.

Wound botulism results when wounds are contaminated with C botulinum spores. Wound botulism has developed following traumatic injury that involved soil contamination, among injection drug users (particularly those who use black-tar heroin[2] ), and after cesarean delivery. The wound may appear deceptively benign. Traumatized and devitalized tissue provides an anaerobic medium for the spores to germinate into vegetative organisms and to produce neurotoxin, which then disseminates hematogenously. The nervous, endocrine, and metabolic systems are predominantly affected. Symptoms develop after an incubation period of 4-14 days, with a mean of 10 days. The clinical symptoms of wound botulism are similar to those of foodborne botulism except that gastrointestinal symptoms (including nausea, vomiting, diarrhea) are uncommon.

Frequency

United States

In the United States, approximately 154 cases of botulism are reported annually to the Centers for Disease Control and Prevention (CDC). Infant botulism accounts for nearly 75% of all botulism cases.

The incidence of foodborne botulism is approximately 24 cases per year. The incidence of wound botulism is 3 cases per year. The incidence of infant botulism is 71 cases per year, with a mean age of 3 months.

Toxin A is found predominantly west of the Mississippi River. Toxin B is found most commonly in the eastern United States. Toxin E is found in northern latitudes, such as the Pacific Northwest, the Great Lakes region, and Alaska. The frequency of botulism in native Alaskans is among the highest in the world.[3] Toxin E outbreaks are frequently associated with fish products.

International

Human botulism is found worldwide. Spores from C botulinum strains that produce type A or B toxins are distributed widely in the soil and have been found throughout the world. Toxin type B is commonly found in Europe. Toxin G was originally isolated in Switzerland.

Mortality/Morbidity

Mortality rates vary based on the age of the patient and the type of botulism. Foodborne botulism carries an overall mortality rate of 5-10%. Wound botulism carries a mortality rate that ranges from 15-17%. The risk of death due to infant botulism is usually less than 1%.

The recovery period from botulism is often prolonged (30-100 d). Some patients demonstrate residual weakness or autonomic dysfunction for 1 year after the onset of the illness. However, most patients achieve full neurologic recovery. Permanent deficits may occur in those who sustain significant hypoxic insults.

Sex

Wound botulism is more common in males. Foodborne botulism has no sexual predilection.

Age

Foodborne botulism and wound botulism predominately occur in adults. The mean age of infant botulism is 3 months.

 

Presentation

History

Following the onset of symptoms, botulism quickly progresses over several days. The magnitude of the neuromuscular impairment can advance hourly. Persons who survive this phase eventually stabilize and then recover over a period of days to months. The mechanism of recovery is not fully understood but requires the generation of new presynaptic axons and the formation of new synapses, as the original synapses are permanently affected. As with tetanus, recovery from botulism does not confer long-term immunity. Rare reports have described a second episode in the same patient.

Foodborne botulism

Foodborne botulism should be suspected in patients who present with an acute gastrointestinal illness associated with neurologic symptoms. Symptoms usually appear within 12-36 hours following consumption of contaminated food products. The severity of the illness varies from mild to severe, but death can occur within 24 hours.

The incubation period is usually 18-36 hours. Depending on toxin dose, the incubation period ranges from 2 hours to 8 days. The onset of symptoms can be abrupt or can evolve over several days.

Wound botulism

Patients with wound botulism typically have a history of traumatic injury with wounds that are contaminated with soil.

Since 1994, the number of patients with wound botulism who have a history of chronic intravenous drug abuse has increased dramatically. In most cases, black-tar heroin has been the implicated vehicle. A study by Yuan et al followed 17 heroin users who had recurrent botulism after using black-tar heroin. Physicians need to be alert to recognize botulism, especially in patients who use black-tar heroin or in those with a history of injection drug–associated botulism.[4]

Rare cases of wound botulism after cesarean delivery have been documented.

Aside from a longer incubation period, wound botulism is similar to foodborne botulism. The incubation period of wound botulism ranges from 4-14 days, with a mean of 10 days. Unlike foodborne botulism, wound botulism causes no gastrointestinal symptoms. Patients may be febrile, but this is more likely due to the wound infection rather than the wound botulism. In many cases, the wound appears benign.

Adult intestinal toxemia

Adult intestinal toxemia results from enteric colonization with C botulinum that progresses to toxin production. The pathophysiology of the changes in the gastrointestinal flora that facilitate colonization is unclear.[5]

Iatrogenic botulism due to accidental overdose of botulinum toxin (Botox)

Cases of botulism due to Botox overdosage have been reported. Symptoms vary and can include dysphagia, ptosis, and diplopia, as well as more severe presentations of systemic weakness or muscle paralysis.[5]

Physical

More than 90% of patients with botulism have 3-5 of the following signs or symptoms: nausea, vomiting, dysphagia, diplopia, dilated/fixed pupils, and an extremely dry mouth unrelieved by drinking fluids.

Generally, botulism progresses as follows:

  • Preceding or following the onset of paralysis are nonspecific findings such as nausea, vomiting, abdominal pain, malaise, dizziness, dry mouth, dry throat, and, occasionally, sore throat. Except for nerves I and II, the cranial nerves are affected first.

  • Cranial nerve paralysis manifests as blurred vision, diplopia, ptosis, extraocular muscle weakness or paresis, fixed/dilated pupils, dysarthria, dysphagia, and/or suppressed gag reflex. Additional neurologic manifestations include symmetric descending paralysis or weakness of motor and autonomic nerves.

  • Respiratory muscle weakness may be subtle or progressive, advancing rapidly to respiratory failure. Progressive muscle weakness occurs and often involves the muscles of the head and neck, as well as intercostal diaphragmatic muscles and those of the extremities.

The autonomic nervous system is also involved. Manifestations of this include the following:

  • Paralytic ileus advancing to severe constipation

  • Gastric dilatation

  • Bladder distention advancing to urinary retention

  • Orthostatic hypotension

  • Reduced salivation

  • Reduced lacrimation

Other neurologic findings include the following:

  • Changes in deep tendon reflexes, which may be either intact or diminished

  • Incoordination due to muscle weakness

  • Absence of pathologic reflexes and normal findings on sensory and gait examinations

  • Normal results on mental status examination

Many patients with foodborne botulism and wound botulism are afebrile.

Causes

Wound botulism

Causes of wound botulism have been associated with traumatic injury involving contamination with soil, chronic abuse of intravenous drugs (eg, black-tar heroin), and cesarean delivery. Wound botulism illness can occur even after antibiotics are administered to prevent wound infection.

Foodborne botulism

Foodborne botulism results from the ingestion of preformed neurotoxins; A, B, and E are the most common. On average, 24 cases of foodborne botulism are reported annually.

High-risk foods include home-canned or home-processed low-acid fruits and vegetables; fish and fish products; and condiments, such as relish and chili peppers.

Commercially processed foods and improperly handled fresh foods are occasionally associated with botulism outbreaks.

Outbreaks of foodborne botulism in restaurants, schools, and private homes have been traced to uncommon sources, such as commercial pot-pies, baked potatoes,[6] beef stew, turkey loaf, sautéed onions, chopped garlic in oil,[7] and cheese sauce.

 

DDx

Diagnostic Considerations

The diseases most frequently confused with botulism are those that produce generalized weakness. Differentiating botulism from other diseases is essential for early initiation of therapy. Botulism should be considered in patients who are afebrile and mentally intact and who have symmetric descending paralysis without sensory findings. The diagnosis should be suspected on clinical grounds in the context of an appropriate history. Other conditions often confused with botulism include the following:

  • Guillain-Barré syndrome

  • Fisher variant of Guillain-Barré syndrome

  • Myasthenia gravis

  • Lambert-Eaton syndrome

  • Poliomyelitis

  • Tick paralysis

  • Cerebrovascular disease of the brainstem

  • Basilar artery stroke

  • Encephalitis

  • Diphtheria

  • Neurasthenia

  • Progressive external ophthalmoplegia

  • Intracranial mass lesions

  • Drugs, penicillamine

  • Aminoglycosides: Very large doses can induce neuromuscular blockade.

  • Poisonings by atropine, scopolamine, organophosphate insecticides, shellfish, amanita mushrooms, carbon monoxide, methyl alcohol, methyl chloride, and sodium fluoride

  • Congenital neuropathy or myopathy

Differential Diagnoses

 

Workup

Laboratory Studies

Laboratory tests are not helpful in the routine diagnosis of botulism.

WBC counts and erythrocyte sedimentation rates are normal.

Cerebrospinal fluid is normal, except for occasional mild elevations in protein concentration.

A mouse neutralization bioassay confirms botulism by isolating the botulism toxin.

Toxin may be identified in serum, stool, vomitus, gastric aspirate, and suspected foods. C botulinum may be grown on selective media from samples of stool or foods. Note that the specimens for toxin analysis should be refrigerated, but culture samples of C botulinum should not be refrigerated.

Because intestinal carriage is rare, identifying the organism or its toxin in vomitus, gastric fluid, or stool strongly suggests the diagnosis. Isolation of the organism from food without toxin is insufficient grounds for the diagnosis. Only experienced personnel who have been immunized with botulinum toxoid should handle the specimens. Because the toxin may enter the blood stream through the eye or via small breaks in the skin, precaution is warranted.

Wound cultures that grow C botulinum suggest of wound botulism.

Imaging Studies

Imaging studies are generally not useful in the diagnosis of botulism.

The only potential role for imaging studies (eg, CT scan, MRI) would be to rule out CNS pathology, such as intracranial mass lesions, cerebrovascular disease of the brainstem, or basilar artery stroke, in patients in whom the presentation is atypical or vague.

Other Tests

Patients with botulism may have mild nonspecific abnormalities on electrocardiography.

Results from nerve conduction studies are normal, and electromyography (EMG) reveals reduced amplitude of compound muscle action potentials.

EMG may be useful in establishing a diagnosis of botulism, but the findings can be nonspecific and nondiagnostic, even in severe cases. Characteristic findings in patients with botulism include brief low-voltage compound motor-units, small M-wave amplitudes, and overly abundant action potentials. An incremental increase in M-wave amplitude with rapid repetitive nerve stimulation may help to localize the disorder to the neuromuscular junction. Single-fiber EMG may be a more useful and sensitive method for the rapid diagnosis of botulism intoxication, particularly in the absence of signs of general muscular weakness.

The results of the edrophonium chloride, or Tensilon, test for myasthenia gravis may be falsely positive in patients with botulism. If positive, it is typically much less dramatically positive than in patients with myasthenia gravis.

 

Treatment

Medical Care

On March 22, 2013, the FDA approved the first botulism antitoxin that can neutralize all 7 known botulinum nerve toxin serotypes. The heptavalent antitoxin is derived from horse plasma and is the only drug available for treating botulism in patients older than 1 year, including adults. It is also the only available drug for treating infant botulism that is not caused by nerve toxin type A or B.[8, 9, 10, 11]

Rigorous and supportive care is essential in patients with botulism.

Meticulous airway management is paramount, as respiratory failure is the most important threat to survival in patients with botulism.

Patients with symptoms of botulism or known exposure should be hospitalized and closely observed.

Spirometry, pulse oximetry, vital capacity, and arterial blood gases should be evaluated sequentially.

Respiratory failure can occur with unexpected rapidity.

Intubation and mechanical ventilation should be strongly considered when the vital capacity is less than 30% of predicted, especially when paralysis is progressing rapidly and hypoxemia with hypercarbia is present.

Many patients require intubation and ventilatory support for a few days to months.

Tracheostomy may prove necessary to manage secretions.

Patients with bowel sounds are administered cathartics and enemas to remove unabsorbed botulinum toxin from the intestine.

Magnesium salts, citrate, and sulfate should not be administered because magnesium can potentiate the toxin-induced neuromuscular blockade.

Stress ulcer prophylaxis is also a standard component of intensive care management.

If an ileus is present, nasogastric suction and intravenous hyperalimentation are very helpful supportive measures. If no ileus is present, tube feeding can be used for nutritional supplementation.

A Foley catheter is often used to treat bladder incontinence. This must be monitored conscientiously and changed regularly.

Measures to reduce the risk of nosocomial infections include the following:

  • Close observation for hospital-acquired infections, especially pneumonia (particularly aspiration pneumonia), is necessary, as is precaution to prevent aspiration. Aggressive pulmonary toilet with clearance of secretions, ventilatory support, and incentive spirometry are typically used.

  • Close observation for urinary tract infection is essential. Foley catheters should be changed on a regular basis.

  • Meticulous skin care is required to prevent decubital ulcers and skin breakdown.

  • Careful attention to peripheral and central intravenous catheters with regular site rotation to reduce the risks of thrombophlebitis, cellulitis, and line infections should be part of the supportive care.

  • Deep venous thrombosis (DVT) prophylaxis is also a standard component of intensive care management.

Surgical Care

Wound botulism requires incision and thorough debridement of the infected wound, antitoxin therapy, and high-dose intravenous penicillin therapy.

Consultations

A nutritionist should be consulted for hyperalimentation and tube-feeding recommendations and monitoring.

Physical and occupational therapists are needed to work on range-of-motion exercises and assisted ambulation, as tolerated.

A psychiatrist and/or a psychologist is recommended for counseling, as needed; patients with prolonged hospitalization, slow recovery, and complications from the disease or from extended hospitalization are at increased risk for depression.

Pastoral care is recommended, as needed.

Physical medicine and rehabilitation specialists may be helpful in coordinating long-term rehabilitation planning once sustained recovery has begun.

Diet

Nasogastric suction and intravenous hyperalimentation are important when an ileus is present. If no ileus is present or when the ileus resolves, tube feeding can be used for nutritional supplementation.

Oral intake should be reinstituted gradually under the following conditions:

  • Respiratory status is stable without mechanical ventilation.

  • Swallowing safety has been assessed and confirmed with a swallowing study, as appropriate.

  • Ileus has resolved.

Activity

Bedrest is initially required.

Increase activity as tolerated.

 

Medication

Medication Summary

Antibiotics are useful in wound botulism, but they have no role in foodborne botulism.

Antibiotics

Class Summary

When botulism develops following a wound infection, antibiotic therapy and meticulous debridement of the wound are essential.

Penicillin G (Pfizerpen)

Preferred drug of choice for wound botulism. Interferes with synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms.

Chloramphenicol (Chloromycetin)

Alternate to penicillin. Binds to 50S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. Effective against gram-negative and gram-positive bacteria.

Clindamycin (Cleocin)

Alternative to penicillin. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Antitoxins

Class Summary

These agents are essential in the treatment of foodborne botulism and wound botulism. Heptavalent antitoxin (toxins A through G) is available at the Centers for Disease Control and Prevention (CDC). The CDC phone number is (770) 488-7100. Twenty percent of patients experience some degree of serum sickness or hypersensitivity reaction, and anaphylaxis can also occur. Patients who react to a test dose must be desensitized. Because of the risk of adverse reactions, prophylactic antitoxin is not recommended in patients who are exposed to botulism toxin but who have no symptoms. These patients may undergo gastric lavage or induced vomiting in an attempt to eliminate the toxin prior to absorption.

Botulinum antitoxin, heptavalent (HBAT)

Antitoxin indicated for naturally occurring noninfant botulism. Equine-derived antitoxin that elicits passive antibody (ie, immediate immunity) against Clostridium botulinum toxins A, B, C, D, E, F, and G.

Each 20-mL vial contains equine-derived antibody to the 7 known botulinum toxin types (A through G) with the following nominal potency values: 7500 U anti-A, 5500 U anti-B, 5000 U anti-C, 1000 U anti-D, 8500 U anti-E, 5000 U anti-F, and 1000 U anti-G.

Replaces licensed bivalent botulinum antitoxin AB (BAT-AB) and investigational monovalent botulinum antitoxin E (BAT-E). To obtain, contact CDC Emergency Operations Center; telephone: (770) 488-7100. Product to be stored in Strategic National Stockpile for emergency preparedness and responses.

 

Follow-up

Further Outpatient Care

The most significant improvements in ventilatory and upper airway muscle strength occur over the first 12 weeks, and, in some patients, recovery may not be complete for as long as a year. Close follow-up is crucial.

Follow-up with other consultants, such as physical medicine and rehabilitation specialists, physical and occupational therapists, nutritionists, and psychiatrists, should be obtained as needed.

Further Inpatient Care

Recovery of ventilatory and upper airway muscle strength in patients who develop respiratory failure is most significant over the first 12 weeks. The time for recovery typically ranges from 30-100 days. Artificial respiratory support may be required for months in severe cases.

Inpatient & Outpatient Medications

When botulism develops following a wound infection, antibiotic therapy and meticulous debridement of the wound are essential.

Penicillin is the drug of choice.

Clindamycin and chloramphenicol are reasonable second-line agents.

Transfer

Transfer is indicated if the patient's condition continues to deteriorate or if the initial hospital is unable to manage the complexities involved.

Deterrence/Prevention

Prompt notification of public health authorities regarding a suspected case of botulism may prevent further consumption of a contaminated home-canned or commercial food product.

Foodborne botulism is best prevented by strict adherence to recommended home-canning techniques. High-temperature pressure cooking is essential to ensure spore elimination from low-acid fruits and vegetables. Although boiling for 10 minutes kills bacteria and destroys the heat labile botulism toxin, the spores are resistant to heat and can survive boiling for 3-5 hours. Food contaminated by botulism toxins usually has a putrefactive odor; however, contaminated food may also look and taste normal. Hence, terminal heating of toxin-containing food can prevent illness and is an important preventive measure.

Wound botulism due to intravenous drug abuse can be prevented by cessation of drug use.

Wound botulism is best prevented by prompt thorough debridement of contaminated wounds. Prophylactic use of antibiotics after trauma cannot be relied on to prevent wound botulism.

Complications

Nosocomial infections

Hospital-acquired pneumonia, especially aspiration pneumonia, can occur. Atelectasis and poor secretion clearance also increase the risk of hospital-acquired pneumonia.

Urinary tract infection can occur from in-dwelling Foley catheters.

Skin breakdown and decubitus formation can occur.

Thrombophlebitis, cellulitis, and line infections can occur. These patients often have peripheral and central intravenous catheters for prolonged periods.

Fungal infections can occur; the predisposing factors include prolonged hospitalization, parenteral nutrition, and central venous catheters. DVT prophylaxis is essential to reduce the risk of these potential complications. DVT and pulmonary embolism (PE) are potential complications because patients can be bedridden for weeks to months.

Stress ulcers can occur and are common in the intensive care unit setting. Stress ulcer prophylaxis is essential to reduce the risk of this potential complication.

Other potential complications

Other potential complications include the following:

  • Hypoxic tissue damage can lead to permanent neurologic deficits.

  • Death

Prognosis

Botulism due to type A toxin is generally more severe than that caused by type B or E.

Mortality rates vary based on the age of the patient and the type of botulism. Foodborne botulism carries an overall mortality rate of 5-10%. Botulism carries a higher mortality rate in patients older than 60 years than in younger patients. Wound botulism carries a mortality rate that ranges from 15-17%. The risk of death due to infant botulism is usually less than 1%.

The recovery period ranges from 30-100 days. Artificial respiratory support may be required for months in severe cases. Full neurologic recovery usually occurs. Hypoxic insults, although infrequent, can result in permanent deficits. Some patients experience residual weakness and autonomic dysfunction for as long as a year after disease onset.

Mortality is due to the following:

  • Delayed diagnosis and respiratory failure

  • Hospital complications such as nosocomial infections (usually pneumonia)

Patient Education

When preserving food at home, kill C botulinum spores by pressure cooking at 250°F (120°C) for 30 minutes. The toxin can be destroyed by boiling for 10 minutes or cooking at 175°F (80°C) for 30 minutes. Do not eat or taste food from bulging cans. Discard food that smells bad.

Cessation of intravenous drug use prevents wound botulism due to this vehicle.

 

Questions & Answers

Overview

What are the main clinical presentations of botulism?

What are the signs and symptoms of botulism?

How does botulism progress?

What are the autonomic nervous system findings characteristic of botulism?

What are the neurologic findings characteristic of botulism?

How is botulism diagnosed?

Which EMG findings are characteristic of botulism?

What is included in supportive care for botulism?

How is wound botulism treated?

How are nosocomial infections prevented in botulism?

What is botulism?

What is the pathophysiology of botulism?

What is the prevalence of botulism in the US?

What is the global distribution of C botulinum strains?

What is the mortality and morbidity associated with botulism?

What are the sexual predilections of botulism?

Which age groups have the highest prevalence of botulism?

Presentation

What causes adult intestinal toxemia botulism?

Which clinical history findings are characteristic of botulism?

Which clinical history findings are characteristic of foodborne botulism?

Which clinical history findings are characteristic of wound botulism?

What are the signs and symptoms of iatrogenic botulism from an overdose of botulinum toxin (Botox)?

How do the physical findings of botulism change as the disease progresses?

What are the autonomic nervous system signs and symptoms of botulism?

What are neurologic signs and symptoms of botulism?

What causes wound botulism?

What causes foodborne botulism?

DDX

Which conditions are included in the differential diagnoses of botulism?

What are the differential diagnoses for Botulism?

Workup

What is the role of lab tests in the workup of botulism?

What is the role of imaging studies in the workup of botulism?

What is the role of electrocardiography in the workup of botulism?

What is the role of NCS and EMG in the workup of botulism?

How is myasthenia gravis differentiated from botulism?

Treatment

How is botulism treated?

How is the risk for nosocomial infections reduced during the treatment of botulism?

What is the role of surgery in the treatment of botulism?

Which specialist consultations are beneficial to patients with botulism?

How is oral intake reinstituted following the treatment of botulism?

Which activity modifications are used in the treatment of botulism?

Medications

What is the role of medications in botulism treatment?

Which medications in the drug class Antitoxins are used in the treatment of Botulism?

Which medications in the drug class Antibiotics are used in the treatment of Botulism?

Follow-up

What is included in long-term monitoring of botulism?

How long does it take to recover from botulism?

What is the role of antibiotics in botulism treatment?

When is patient transfer indicated for botulism treatment?

How is botulism prevented?

What are the possible complications of botulism?

What is the prognosis of botulism?

What is included in patient education about botulism?